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Abstract

Introduction

Takotsubo cardiomyopathy (TC), also known as stress cardiomyopathy, and broken heart syndrome is characterized by transient left ventricular (LV) apical akinesis with symptoms mimicking acute coronary syndrome. The first case was described by Sato et al. in Japan.1 The Japanese word “takotsubo” translates to “octopus pot” describing the shape of the left ventricle during systole. TC can be triggered by a “broken heart” including death of a loved one, constant anxiety, surgery, or critical illness etc. Prevalence is around 2% to 3% with over 90% in postmenopausal women aged between 58 and 75. Its pathogenesis remains unclear. Some postulated that excess catecholamine released during stress can induce an exaggerated sympathetic response precipitating severe, reversible LV dysfunction in patients without coronary disease.2 Whether there is a genetic component is not well understood. There are a few reported cases of Takotsubo in family members, one case of two sisters and another mother-daughter pair.3,4 Recurrence of the syndrome in the same patient, although rare, can occur and suggests a genetic predisposition.5 Majority of patients regain normal ventricular function within one to four weeks if they survive the acute episode. Hospital mortality rates range from 0 to 8 %. However, one major complication is the risk of intraventricular thrombus formation and systemic embolization. Data is lacking to guide anticoagulation for LV thrombus prevention in patients with stress cardiomyopathy.

Case Presentation

Mrs. S is a 62 year old woman with a prior history of TC with full recovery, hyperlipidemia, and gastroesophageal reflux disease presented with chest pain radiating to her left shoulder. She was under significant financial stress during that week. Her pain was unrelieved with aspirin or sublingual nitroglycerin. In the emergency room, her electrocardiogram showed ST segment elevations in leads V2-V6 (Figure 1) with Troponin T 1.49ng/mL. She was immediately started on heparin and nitroglycerin drips and rushed to the catheterization laboratory. Coronary angiography did not reveal significant coronary disease but incidentally found elevated pulmonary wedge pressures. Upon transfer to the cardiac intensive unit, Mrs. S became hypotensive and norepinephrine was started. Her transthoracic echocardiogram (TTE) revealed moderately decreased LV systolic function with an estimated ejection fraction (EF) of 35%, with segmental wall motion abnormalities, mid and distal akinesis of the LV and hyperkinesis of basal LV. There was a late-peaking LV outflow tract gradient of 77 mm Hg consistent with severe, dynamic left ventricular outflow tract (LVOT) obstruction.

She had a prior episode of TC when her husband passed away three years ago. She also has a twin sister who suffered from TC a year ago when she lost her job. Unlike Mrs. S, she did not fully recover and required long term heart failure management.

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